Cited by 136Erythropoietin and Anemia TreatmentCancer, Hypoxia, and MetabolismEar and Head Tumors

Mutations in the VHL gene in sporadic apparently congenital polycythemia

Pastore, Yves D., Jelinek, Jaroslav, Ang, Sonny, Guan, Yongli, Liu, Enli, Jedlickova, Katerina, Krishnamurti, Lakshmanan, Prchal, Josef T.·2003·Blood

Abstract

The congenital polycythemic disorders with elevated erythropoietin (Epo) have been until recently an enigma, and abnormality in the hypoxia-sensing pathway has been hypothesized as a possible mechanism. The tumor suppressor von Hippel-Lindau (VHL) participates in the hypoxia-sensing pathway, as it binds to the proline-hydroxylated form of the hypoxia-inducible factor 1alpha (HIF-1alpha) and mediates its ubiquitination and proteosomal degradation. The loss of VHL function may result in the accumulation of HIF-1alpha and overproduction of HIF-1 downstream target genes including Epo. VHL syndrome is an autosomal dominant disorder predisposing to the development of tumors, due to inherited mutations in the VHL gene. Some rare patients with VHL syndrome have polycythemia, which has been attributed to Epo production by a tumor. It was recently found that homozygosity for the VHL Arg200Trp mutation is the cause of Chuvash polycythemia, an autosomal recessive polycythemic disorder characterized by elevated serum Epo and hypersensitivity of erythroid cells to Epo. We evaluated the role of VHL in 8 children with a history of polycythemia and an elevated serum Epo level and found 3 different germline VHL mutations in 4 of them. One child was homozygous for the Arg200Trp VHL mutation, and another compound heterozygous for the Arg200Trp and the Val130Leu mutations. Two children (siblings) were heterozygous for an Asp126Tyr mutation, one of them fulfilling some criteria of VHL syndrome. We propose that mutations of the VHL gene represent an important cause of pediatric sporadic polycythemias with an inappropriately high serum Epo concentration.

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Crossref · 10.1182/blood-2002-06-1843

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Authors
Pastore, Y. D., Jelinek, J., Ang, S., Guan, Y., Liu, E., Jedlickova, K., Krishnamurti, L., & Prchal, J. T.
Affiliations
  • University of Minnesota (US)
  • From the Texas Children's Cancer Center and Hematology Service, Houston; Baylor College of Medicine and Veterans Administration Hospital, Houston, TX; and University of Minnesota, Minneapolis.
Venue
Blood
Published
2003-02-15
Volume
101
Issue
4
Pages
1591-1595
ISSN
  • 0006-4971 (ISSN-L)
  • 1528-0020
OpenAlex
W2000596340
Cited by
136
References
28
Citations by year
2026: 1 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 5 · 2015: 6 · 2014: 5 · 2013: 9 · 2012: 4
FWCI
7.26
Type
journal article
Language
en
Open access
closed
Locations
  • Blood (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Heart, Lung, and Blood Institute (R01HL5007-08, R01HL066333, R01HL66333-01)
Topics
  • Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Health Sciences › Medicine › Oncology › Ear and Head Tumors
Keywords
VHL gene, von Hippel-Lindau disease, erythropoietin, hypoxia-inducible factor-1α, germline mutations, compound heterozygosity, tumor suppressor
MeSH terms
Adolescent, Adult, Arginine, Aspartic Acid, Base Sequence, Child, Child, Preschool, DNA Mutational Analysis, Erythropoietin, Female, Heterozygote, Homozygote, Humans, Leucine, Ligases, Male, Mutation, Pedigree, Polycythemia, Tryptophan, Tyrosine, Valine, Erythroid Precursor Cells, Sequence Analysis, DNA, Tumor Suppressor Proteins, Ubiquitin-Protein Ligases, Von Hippel-Lindau Tumor Suppressor Protein

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